Biogenesis, functions and clinical significance of circRNAs in gastric cancer

Shan, Chan; Zhang, Yinfeng; Hao, Xiaodan; Gao, Jinling; Chen, Xinzhe; Wang, Kun

doi:10.1186/s12943-019-1069-0

Cited by 167 publications

(141 citation statements)

References 146 publications

(161 reference statements)

Supporting

Mentioning

137

Contrasting

Order By: Relevance

“…These data suggested that circRNA_100269 could inhibit the proliferation, migration and invasion while inducing the cell cycle arrest and apoptosis of GC cells by suppressing PI3K/Akt signaling pathway. In consistence with our ndings, recent studies also reported circRNAs including circNHSL1 and circNF1 could be novel gene regulators in GC, which can affect tumor progression through various signaling pathways (22)(23)(24)(25)(26)(27). Taken all together, our results revealed the essential roles of circRNA_100269/PI3K/Akt signaling on the modulation of GC progression.…”

Section: Discussionsupporting

confidence: 89%

Upregulated circRNA_100269 suppresses the growth and metastasis of gastric cancer by inactivating PI3K/Akt signaling pathway

wang

liu

2020

Preprint

View full text Add to dashboard Cite

Background: The expression of circRNA_100269 in gastric cancer (GC) tissues and cells, together with its regulatory roles on GC cells were investigated. Methods: The levels of circRNA_100269 in GC and matched para-carcinoma tissues, as well as in human GC cell lines and normal gastric epithelial cells were evaluated using RT-qPCR. The models with overexpression or knockdown of circRNA_100269 were generated using lentiviral vectors. Cell viability was examined using MTT assay; cell migration and invasive activity were determined by wound healing and Transwell assay. Cell cycle arrest and apoptosis were assessed; molecules involved in PI3K/Akt signaling, apoptosis and EMT were evaluated using RT-qPCR and immunoblotting. Tumour growth and expression of relevant proteins were examined in circRNA_100269 knockout mice. Results: The results indicated the expression of circRNA_100269 was dramatically decreased in GC samples compared with para-carcinoma tissues (p<0.05), while the levels of PI3K were notably increased (p<0.05). Moreover, the level of circRNA_100269 was relevant to histology grade and occurrence of metastasis in GC patients (p<0.05), where circRNA_100269 and PI3K was inversely correlated (p<0.05). Additionally, circRNA_100269 was downregulated in GC cells compared with normal gastric epithelial cells. Overexpressed circRNA_100269 remarkably suppressed the proliferation, migration, invasion and EMT of GC cells (p<0.05), induced cell cycle arrest at G0/G1 phase and promoted cell apoptosis (p<0.05). In addition, PI3K/Akt signaling was involved in circRNA_100269-mediated proliferation, migration, invasion, EMT and apoptosis in GC cells (p<0.05). Knockdown of circRNA_100269 also significantly promoted tumor growth in vivo (p<0.05). Conclusions: the data of the present study suggested that the expression level of circRNA_100269 was decreased in GC tissues and cells. In addition, circRNA_100269 inhibited the progression of GC by suppressing PI3K/Akt signaling. Therefore, circRNA_100269/PI3K/Akt axis may be a potential therapeutic target for GC treatment.

show abstract

Section: Discussionsupporting

confidence: 89%

Upregulated circRNA_100269 suppresses the growth and metastasis of gastric cancer by inactivating PI3K/Akt signaling pathway

wang

liu

2020

Preprint

View full text Add to dashboard Cite

show abstract

“…GC is a public problem with high incidence and mortality [21]. CircRNAs have the critical clinical significance in GC [22]. The former work suggested that down-regulation of hsa_circ_0003159 had the potential clinical value in GC [10].…”

Section: Discussionmentioning

confidence: 99%

Hsa_circ_0003159 inhibits gastric cancer progression by regulating miR-223-3p/NDRG1 axis

Wang

Lin

et al. 2020

Cancer Cell Int

View full text Add to dashboard Cite

Background: Abnormally expressed circular RNAs (circRNAs) are implicated in the development and treatment of gastric cancer (GC). Previous study has reported that hsa_circ_0003159 is expressed in GC. However, the role and mechanism of hsa_circ_0003159 in GC progression remain unclear. Methods: GC tissues and normal tissues were harvested from 55 patients in this study. The levels of hsa_ circ_0003159, microRNA (miR)-223-3p and N-myc downstream regulated gene 1 (NDRG1) were measured by quantitative real-time polymerase chain reaction or western blot. Cell proliferation, migration, invasion and apoptosis were determined by cell counting kit (CCK)-8, transwell assay, flow cytometry and western blot, respectively. The target association of miR-223-3p-hsa_circ_0003159 and miR-223-3p-NDRG1 was explored by dual-luciferase reporter assay. Xenograft model was established to assess the roles of hsa_circ_0003159 in GC in vivo. Results: Hsa_circ_0003159 was lowly expressed in GC tissues and cells and mainly presented in the cytoplasm. Low expression of hsa_circ_0003159 was associated with lower overall survival and disease-free survival. Hsa_circ_0003159 overexpression inhibited proliferation, migration and invasion but induced apoptosis in GC cells. MiR-223-3p was a target of hsa_circ_0003159 and abated the effect of hsa_circ_0003159 on proliferation, migration, invasion and apoptosis in GC cells. Hsa_circ_0003159 promoted NDRG1 expression by competitively sponging miR-223-3p. Knockdown of NDRG1 reversed the suppressive effect of hsa_circ_0003159 on GC progression. Besides, hsa_circ_0003159 decreased GC cell xenograft tumor growth by regulating miR-223-3p and NDRG1. Conclusion: Hsa_circ_0003159 suppressed proliferation, migration, invasion and xenograft tumor growth but promoted apoptosis by decreasing miR-223-3p and increasing NDRG1 in GC, indicating a novel target for treatment of GC.

show abstract

“…However, CDR1as also functions in non-brain tissues, such as in islet and HCC cells, where it targets miR-7 expression (Xu et al, 2015;Yu et al, 2016), and in bladder cancer tissues where it sponges miR-135a (Li P. et al, 2018). With development of the ceRNA hypothesis, additional circRNAs have been discovered to act as miRNA sponges in cells (Zheng et al, 2016;Shan et al, 2019;Wang et al, 2019).…”

Section: Functions Of Circrnas Circrnas Serve As Sponges For Mirnasmentioning

confidence: 99%

Structure, Regulation, and Function of Linear and Circular Long Non-Coding RNAs

Qin

Zhang

2020

Front. Genet.

View full text Add to dashboard Cite

Long non-coding RNAs (lncRNAs), including linear lncRNAs and circular RNAs (circRNAs), exhibit a surprising range of structures. Linear lncRNAs and circRNAs are generated by different pathways. Linear lncRNAs perform functions that depend on their specific sequences, transcription, and DNA elements of their gene loci. In some cases, linear lncRNAs contain a short open reading frame encoding a peptide. circRNAs are covalently closed RNAs with tissue-specific and cell-specific expression patterns that have recently been extensively investigated. Pioneering work focusing on their biogenesis and functional characterization indicates that circRNAs regulate cell development via multiple mechanisms and play critical roles in the immune system. Furthermore, circRNAs in exosomes function on target cells. As with linear lncRNAs, specific circRNAs can also be translated. In this review, we summarize current understanding and highlight the diverse structure, regulation, and function of linear lncRNAs and circRNAs.

show abstract

Biogenesis, functions and clinical significance of circRNAs in gastric cancer

Cited by 167 publications

References 146 publications

Upregulated circRNA_100269 suppresses the growth and metastasis of gastric cancer by inactivating PI3K/Akt signaling pathway

Upregulated circRNA_100269 suppresses the growth and metastasis of gastric cancer by inactivating PI3K/Akt signaling pathway

Hsa_circ_0003159 inhibits gastric cancer progression by regulating miR-223-3p/NDRG1 axis

Structure, Regulation, and Function of Linear and Circular Long Non-Coding RNAs

Contact Info

Product

Resources

About